PROBLEM SET FOR SGD 9: RESPIRATORY 2

1. Correlate the previously discussed issues with the following clinical states, use figure 21-2 of
Berne & Levy 7th edition:

Section B – Discuss the air resistance, flow, volume in a 23 y/o female with on and off difficulty
breathing with response to SAB2 A (slow acting beta 2 agonist),

WHAT IS….
1. SAB2-A (Short Acting Beta 2 Agonist)
● Lung Bronchodilators
○ β2-Agonists dilate bronchi and are used to treat asthma and chronic
obstructive lung disease.

2. The patient may have asthma which involves both large and small airways and is
characterized by inflammation, predominantly mediated by lymphocytes and eosinophils,
in the airways and reversible airway smooth muscle constriction (bronchospasm)

There are three major signs of asthma:

● Airway blockage. Muscles tighten. It’s harder for air to pass through
● Inflammation . Asthma causes red, swollen bronchial tubes in your lungs. This
inflammation can damage your lungs.
● Airway irritability. People with asthma have sensitive airways that tend to overreact
and narrow when they come into contact with even slight triggers.

WHAT IS AIRWAY RESISTANCE?

Airway resistance is defined as the change of pressure (ΔP) from the alveoli to the mouth
divided by the change in flow rate (V). It is the second major factor that determines rates
of airflow in the airways.

Airflow resistance in the airways (R aw) differs in airways of different size. In moving from the
trachea toward the alveolus, individual airways become smaller while the number of airway
branches increases dramatically.

Raw (AirwayResistance) is equal to the sum of the resistance of each of these airways (i.e., R
aw = R large + R medium + Rsmall )
FACTOR Patient Medical Correlation

AIRWAY RESISTANCE Factors that increase airway resistance include airway mucus,
edema, and contraction of bronchial smooth muscle, all of
which decrease the caliber of the airways.
 1. Patients with asthma have increased mucus production
and viscosity. This causes abnormalities in mucociliary
clearance in the absence of infection.
○ PATHOPHYSIO WILL BE DISCUSSED FURTHER
LATER

2. From Poiseuille’s equation one might conclude that the

major site of airway resistance is in the smallest airways.
However, the major site of resistance along the
bronchial tree is the large bronchi. The smallest airways
contribute very little to the overall total resistance of the
bronchial tree. Bronchi and bronchioles significantly
contribute to airway resistance.

Because of the structure of the bronchial tree, and thus the

pathway for air that contributes to its resistance, it is greatly affected
in OLD.
● In all areas of the trachea and bronchi not occupied by
cartilage plates, the walls are composed mainly of smooth
muscle. Also, the walls of the bronchioles are almost
entirely smooth muscle, with the exception of the most
terminal bronchiole, called the respiratory bronchiole, which
is mainly pulmonary epithelium and underlying fibrous tissue
plus a few smooth muscle fibers.

EXCESSIVE CONTRACTION of the smooth muscle that lines the

bronchial airways will increase airway resistance and make
breathing more difficult.

In addition to the effects of disease, airway resistance is regulated

by various neural and humoral agents.Stimulation of efferent vagal
fibers, either directly or reflexively, increases airway resistance and
decreases anatomic dead space secondary to airway constriction
 FLOW In obstructive lung diseases, such as asthma or chronic bronchitis,
airway resistance is elevated and greater negative pleural
pressure is needed to maintain normal inspiratory flow rates. In
addition to the increase in total inspiratory work (OAECD),
individuals with obstructive lung disease have an increase in
positive pleural pressure during exhalation because of the
increase in resistance and the increased expiratory workload, which
is visualized as area DFO.

VOLUME (steff) One of the most important factors affecting resistance is lung
volume. Increasing lung volume increases the caliber of the
airways. As a result, resistance to airflow decreases with
increasing lung volume, and it increases with decreasing lung
volume.

Airway resistance is significantly increased as lung volume is

reduced.
BOYLE’S LAW = At constant temp, pressure and volume have
an INVERSE relationship
P1V1 = P2V2

Measurements where alveolar and intrapleural pressure can be compared to actual pressure
show the contribution of airway resistance

In healthy individuals, airway resistance is approximately 1 cm H2 O/L · sec.

Factors that increase airway resistance include airway mucus, edema, and contraction of
bronchial smooth muscle, all of which decrease the caliber of the airways.

Reflex stimulation of the vagus nerve by the inhalation of smoke, dust, cold air, or other irritants
can also result in airway constriction and coughing. Agents such as histamine, acetylcholine,
thromboxane A2 , prostaglandin F2 , and leukotrienes (LTB4 , LTC4 , and LTD4 ) are released
by resident (e.g., mast cells and airway epithelial cells) and recruited (e.g., neutrophils and
eosinophils) airway cells in response to various triggers, such as allergens and viral infections.
These agents act directly on airway smooth muscle to cause constriction and an increase in
airway resistance. Inhalation of methacholine, a derivative of acetylcholine, is used to diagnose
airway hyperresponsiveness, which is one of the cardinal features of asthma. Although
everyone is capable of responding to methacholine, airway obstruction develops in patients with
asthma at much lower concentrations of inhaled methacholine.

The density and viscosity of the inspired gas also affect airway resistance. When scuba
diving, gas density rises and results in an increase in airway resistance; this increase can cause
problems for individuals with asthma and obstructive pulmonary disease.
Changes in alveolar and pleural pressure during a tidal volume breath. Inspiration is to the left
of the vertical dotted line and exhalation is to the right. Positive (relative to atmosphere)
pressures are above the horizontal dotted line and negative pressures are below. At points of
no airflow (A and C) alveolar pressure is zero

​Berne Fig 21-2

2. KB is a 30-year old male 10-pack year smoker and asthmatic maintained on a
long-acting beta agonist + inhaled corticosteroid (LABA-ICS) combination. He has had
nighttime symptoms of cough and wheezing for the past 5 days, which were relieved by
B2 agonists delivered by metered dose inhalers (MDI). He has also had episodic
shortness of breath during the day.

a. Explain the symptoms and discuss the pathophysiologic mechanisms involved

Sx Explanation

night time sx (AB) ● Nighttime coughing and wheezing may be due to increase
airway resistance in asthmatic patients at night, which makes
it more difficult for the lungs to take air in and out of it.
● Asthma is associated with a circadian pattern in lung
function, (it is characteristic of asthma that symptoms worsen
in the early hours of the morning around 4:00 am) worst lung
function typically occurring at approximately 4am. Nocturnal
asthma appears to reflect on exaggeration of the effects of
normal changes in neurohormonal activation that have
time-related rhythms

Episodic shortness of ● Incident or acute event with sudden onset that is unpleasant
breath during the day and often causes panic.
(Franco) ● These are often triggered by exertion, for example, climbing
stairs, walking, or even talking
● Due to the hyperresponsiveness of the airways commonly
noted in asthmatics

Obstructive Disease—Asthma (anne)

Asthma is characterized by episodic or chronic wheezing, cough, and a feeling of
tightness in the chest as a result of bronchoconstriction.

3 airway abnormalities are present:

● airway obstruction that is at least partially reversible,
● airway inflammation, and
● airway hyperresponsiveness to a variety of stimuli.

A link to allergy has long been recognized, and plasma IgE levels are often elevated.

1. Proteins released from eosinophils in the inflammatory reaction may damage the
airway epithelium and contribute to the hyperresponsiveness.
2. Leukotrienes are released from eosinophils and mast cells, and can enhance
bronchoconstriction.
3. Numerous other amines, neuropeptides, chemokines, and interleukins have effects on
 bronchial smooth muscle or produce inflammation, and they may be involved in
asthma.

Asthma—Spasmodic Contraction of Smooth Muscles in Bronchioles

Asthma is characterized by spastic contraction of the smooth muscle in the bronchioles,

which partially obstructs the bronchioles and causes extremely difficult breathing. It
occurs in 3 to 5 percent of all people at some time in life.

The usual cause of asthma is contractile hypersensitivity of the bronchioles in response

to foreign substances in the air. In about 70 percent of patients younger than age 30 years,
the asthma is caused by allergic hypersensitivity, especially sensitivity to plant pollens. In
older people, the cause is almost always hypersensitivity to nonallergenic types of irritants in
the air, such as irritants in smog.

The allergic reaction that occurs in the allergic type of asthma is believed to occur in the
following way:
● The typical allergic person tends to form abnormally large amounts of IgE
antibodies, and these antibodies cause allergic reactions when they react with the
specific antigens that have caused them to develop in the first place,
● In asthma, these antibodies are mainly attached to mast cells that are present in the
lung interstitium in close association with the bronchioles and small bronchi. When the
asthmatic person breathes in pollen to which he or she is sensitive (i.e., to which the
person has developed IgE antibodies), the pollen reacts with the mast cell–attached
antibodies and causes the mast cells to release several different substance. Among
them are
○ (a) histamine,
○ (b) slow-reacting substance of anaphylaxis (which is a mixture of leukotrienes),
(c) eosinophilic chemotactic factor, and
○ (d) bradykinin.
● The combined effects of all these factors, especially the slow reacting substance of
anaphylaxis, are to produce
○ (1) localized edema in the walls of the small bronchioles, as well as
secretion of thick mucus into the bronchiolar lumens, and
○ (2) spasm of the bronchiolar smooth muscle.Therefore, the airway
resistance increases greatly.

As discussed earlier in this chapter, the bronchiolar diameter becomes more reduced during
expiration than during inspiration in asthma, caused by bronchiolar collapse during expiratory
effort that compresses the outsides of the bronchioles. Because the bronchioles of the
asthmatic lungs are already partially occluded, further occlusion resulting from the external
pressure creates especially severe obstruction during expiration. That is, the asthmatic
person often can inspire quite adequately but has great difficulty expiring.

Clinical measurements show (1) greatly reduced maximum expiratory rate and (2) reduced
timed expiratory volume. Also, all of this together results in dyspnea, or “air hunger,” which is
discussed later in this chapter.

The functional residual capacity and residual volume of the lung become especially
 increased during the acute asthmatic attack because of the difficulty in expiring air from
the lungs. Also, over a period of years, the chest cage becomes permanently enlarged,
causing a “barrel chest,” and both the functional residual capacity and lung residual volume
become permanently increased.

b. Discuss the role of medications in this setting: (Xena)

● β2 -adrenergic receptors mediate bronchodilation
● β2 -adrenergic agonists have long been the mainstay of “rescue” treatment for mild to
moderate asthma attacks.
● Inhaled steroids are used even in mild to moderate cases to reduce inflammation; they
are very effective, but their side effects can be a problem.
● Agents that block synthesis of leukotrienes or their CysLT1(Cysteinyl leukotriene
receptor 1) receptor inhibit acetylcholine-mediated activation of muscarinic (M) receptors
and blockade Cl − channels and Ca 2+ channels in mast cells have also proved useful in
certain cases

Maintenance treatment with an inhaled corticosteroid (ICS) and a long-acting β2-agonist (LABA)
is recommended for patients whose asthma is not controlled with a low-to-moderate dose of ICS
alone;

hello: hahahahaha haha. In case lang tanungin ni Doc C yung purpose ni corticosteroid; it’s
function is to prevent yung downregulation ng b2 receptor. Since diba medicated, and
regular yung intake ng LAB2-A, so left alone, magdodownregulate yung B2 receptor. So it is to
prevent the downregulation

LABA-ICS combination inhaler -Rhazel

- Long-acting beta agonists in combination with inhaled corticosteroid are indicated in
patients whose nocturnal asthma symptoms are not controlled with inhaled
glucocorticoids alone; they should always be used in combination with an inhaled
glucocorticoid. LABAs can lead to improved overnight lung function but not total
elimination of the nocturnal decrement in lung function. Controller medication

A. Long-acting beta-agonists. These medications relax the muscle bands that

surround your airways. You might hear them called bronchodilators. You’ll take
these medications with an inhaler, even when you have no symptoms. They
include:
■ Formoterol (Foradil)
■ Salmeterol (Serevent

B. Combination inhaler. This device gives you an inhaled corticosteroid and a

long-acting beta-agonist together to ease your asthma. Common ones include:
■ Budesonide and formoterol (Symbicort)
■ Fluticasone and salmeterol (Advair Diskus)
 ■ Fluticasone and vilanterol (Breo)
■ Mometasone and formoterol (Dulera)
B2 agonists via metered dose inhaler - Java
- Short-acting beta agonists in MDIs are the first line of therapy for the quick relief of
acute asthma symptoms. These are known as rescue medicines or rescue
inhalers. SABAs are prescribed for use as-needed, rather than on a routine
basis. Escalating use of a SABA (>6 to 8 puffs per day from a metered dose inhaler or
use exceeding one canister per month) is a warning sign that the patient's underlying
disease activity is inadequately controlled and that additional intervention is warranted.
They are fast acting and metered dose to make sure right amount of dosage is
provided right to the air pipe of the patient, when inhaled.. They loosen the bands
of muscle around your airways and ease symptoms.
■ Albuterol (Accuneb, ProAir, Proventil, Ventolin)
■ Levalbuterol (Xopenex HFA)
PROBLEM SET FOR SGD 10: RESPIRATORY 3

A 60-year old man weighing 50 kg for removal of right lung mass requires one lung ventilation.
The anesthesiologist used a special tube (double lumen) to isolate the left lung. This allows
intraoperative ventilation of the left lung (by using the left port of the tube only) while the right
lung is immobile and collapsed (because the right tube is clamped) which will facilitate surgical
removal of the mass (as shown in the figure on the right). Fifteen minutes into surgery with the
right chest opened and the right lung collapsed, the patient desaturated. He called for help and
the following came and gave various suggestions. Please help elucidate on how the following
interventions can help improve the saturation of the patient.

VENTILATION-PERFUSION RELATIONSHIPS (Xena)

● The ventilation-perfusion ratio (also referred to as the V/Q ratio) is defined as the ratio of
ventilation to blood flow.
● This ratio can be defined for a single alveolus, for a group of alveoli, or for the entire
lung.
● When perfusion exceeds ventilation, the ventilation. perfusion ratio is less than 1
(V/Q <1). Mismatching of pulmonary blood flow and ventilation results in impaired O 2
and CO 2 transfer.
○ In individuals with cardiopulmonary disease, mismatching of pulmonary blood flow and
alveolar ventilation is the most frequent cause of systemic arterial hypoxemia (reduced
blood PO2 ).
● A normal ventilation-perfusion ratio does not mean that ventilation and perfusion to that
lung unit are normal; it simply means that the relationship between ventilation and
perfusion is normal.
Regional Differences in Ventilation/ Perfusion Ratios

● The ventilation-perfusion ratio varies in different areas of the lung.

● In an upright subject, ventilation increases more slowly than blood flow from the
apex of the lung to the base.
● V/Q ratio at the apex of the lung > 1
● V/Q ratio at the base of the lung <1

One lung ventilation

● mechanical separation of the two lungs to allow ventilation of only one lung, while the
other lung is compressed by the surgeon or allowed to passively deflate.
● OLV is indicated when there is collapse of one lung to facilitate surgical exposure for
pulmonary and other thoracic surgeries, or may be used to isolate a pathologic from a
healthy lung to prevent soiling or to allow differential ventilation.
○ Open pulmonary surgery (pneumonectomy, lobectomy)
○ Open pleural surgery etc
● Use double lumen tube

OLV CAUSES CHANGES IN V/Q RATIO

● During normal ventilation (V and Q are well matched anatomically)

○ dependent portions of the lungs receive both greater blood flow (a result of
gravity) and greater ventilation (from gravitational effects on lung compliance).
● The initiation of OLV stops all ventilation to one lung, which would create a 50
percent right-to-left shunt and relative hypoxemia if perfusion were unchanged.
● SHUNT OCCURS = No ventilation but there is perfusion (R to L SHUNT OCCURS)
● However, the actual shunt fraction is usually only 20 to 30 percent for the following
reasons
○ Surgical manipulation of the atelectatic lung obstructs vascular flow to the
non-ventilated lung.
○ Lateral positioning of the patient leads to a gravitational increase in perfusion to
the dependent, ventilated lung.
○ Hypoxic pulmonary vasoconstriction (HPV) modulates the blood flow to hypoxic
regions of the lungs.

RIGHT LUNG - BAD LUNG - DEPENDENT LEFT LUNG - GOOD LUNG - NON
LUNG - VENTILATED LUNG DEPENDENT LUNG - NON VENTILATED
LUNG

● Increasing alveolar ventilation here ● Blood flowing through DOES NOT

DAPAT TAKE PART IN GAS EXCHANGE
○ Leads to decrease arterial ● Remains perfused → Increased shunt
CO2 fraction → decrease oxygenation
https://www.mcgill.ca/anesthesia/files/anesthesia/wk_3c_olv_hypoxia.pdf

1. Senior consultant 1: Turn the patient from supine to left lateral decubitus position.
- Strict lateral decubitus position on the side of the dependent lung = better oxygenation
than semilateral or even supine position
- The lateral position causes expansion of the upper lung and thus improves compliance
of that lung. Because of this, a greater fraction of the tidal volume is distributed towards
the upper lung during both spontaneous breathing and mechanical ventilation.
- Lateral positioning of the patient leads to a gravitational increase in perfusion to the
dependent, ventilated lung.

2. Senior consultant. 2: Stop the surgery and ventilate both lung (two lung ventilation)
(Marcy)

The first step when a patient suffers from hypoxemia (i.e., a drop in pulse oxymetry less
than 90%) during OLV is to stop surgery, increase the inspired oxygen fraction to 100%, and
rapidly restore two-lung ventilation (TLV).

When profound hypoxaemia develops during OLV, it is necessary to treat the problem by
increasing the inspired oxygen to 100% and, on some occasions, ventilating both lungs.That
can be performed with a manual reexpansion of the lung using the hand bag with pure oxygen
flow and an airway pressure limited valve between 20 and 30 cm H2 O; and checks should be
performed (the reexpansion of the deflated lung is visual)
- ventilate both lungs, treat hypoxemia

Strategies to manage hypoxaemia may be divided into three main categories:

● delivery of oxygen to the patient,
● treatment of causes associated with high airway pressure
● management of physiological hypoxaemia.

*Xena summary: Physiological shunt

3. Surgeon: Manual compression of the right lung (Mimi)

Diminished functional residual capacity is associated with alveolar collapse, most commonly in
basal or dependent portions of the lung, making ventilation weaning more difficult and resulting
in excess morbidity and mortality. Since perfusion remains unaltered, an imbalance occurs in
the ventilation/perfusion ratio (V/Q ratio), resulting in arterial hypoxemia.
MCCD maneuver does not require high airways pressure, reducing therefore the risk of
disruption of the alveolocapillary barrier or barotrauma.

Manual chest compression and decompression permits an increase in pulmonary tidal volume
as a consequence of an increased elastic forces in the respiratory system (mainly in the rib
cage) causing greater negative pleural pressure and thus, increased transpulmonary
pressure, generating a greater pressure differential with an increase in flow and, consequently,
greater inspired volume.

The main physiological effects of MCCD maneuver are atelectatic alveolar recruitment and an
increase in functional residual capacity. The use of larger tidal volume than those used by the
mechanical ventilation in some respiratory cycles promote an improvement in the
ventilation/perfusion ratio and a reduction in the shunt, improving oxygenation and reducing the
respiratory effort, without affecting hemodynamic.
- divert perfusion again to the better ventilated lung??

4. Assistant surgeon: Administer intravenous almitrine (a respiratory stimulant) (H)

- Almitrine is a peripheral chemoreceptor agonist that potentiates HPV (hypoxic pulmonary
vasoconstriction) - only in the lungs
- enhances respiration by acting as an agonist of peripheral chemoreceptors
located on the carotid bodies.
- Almitrine at low doses selectively enhances HPV in the non ventilated operative lung
- It decreases intrapulmonary shunt by enhancing HPV and improving gas exchange
- The drug increases arterial oxygen tension while decreasing arterial carbon dioxide
tension
- An adverse effect of almitrine is elevation of pulmonary vascular resistance, which, if
excessive, could potentially induce right ventricular dysfunction.
HPV - vasoconstriction that leads or diverts blood flow away from areas where alveolar oxygen
tension is low → shunt it to better ventilated zones → Improving V/Q relationship
● Decreases blood flow to the non dependent lung
● Decreases shunt by 50→ 30%
● Blood will flow to Left lung (better ventilated lung)
● DIVERT PERFUSION TOWARDS LEFT!
HPV happens in the right lung - to be able to divert perfusion ot the left lung

5. Surgical resident: Allow patient to inhale nitric oxide (KYLE)

- Inhaled nitric oxide (iNO) is an endothelium-derived relaxing factor
- It is a selective pulmonary vasodilator → improve oxygenation in the lungs
- Nitric oxide can be used to decrease intrapulmonary shunt
- Inhaled nitric oxide only accesses the ventilated alveoli, where it causes localized
vasodilation and increases perfusion to the adequately ventilated region of the lung
- Inhaled nitric oxide only improves oxygenation when PEEP (Positive end expiratory
pressure) is high
 - Inhibits HPV

Inhalational nitric oxide dilates blood vessels → will go the left lung → improve V/Q ratio
(increased perfusion)

6. Medical Intern: Ask the surgeon to clamp the right pulmonary artery (BELLA)
- During pneumonectomy, ligation of the pulmonary artery completely eliminates shunt,
thereby maximizing the dependent lung V/Q relationship. Clamping the pulmonary artery
during lobectomy will direct blood to the ventilated lung. This maneuver should be
avoided because reperfusion after total interruption of pulmonary artery blood flow may
injure the lung.
- DIVERT BLOOD TOWARDS THE BETTER VENTILATED LEFT LUNG!
- Right lung has a shunt, clamping will improve the ventilation of the left lung

LIGATION OF PA IN THE NON VENTILATED LUNG → DECREASE BLOOD FLOW TO THE

GOOD LUNG → Eliminate shunt → improving V/Q relationship of dependent lung by
increasing blood flow to the dependent lung

7. Nurse: Proceed with the surgery. Administer continuous oxygen flow at two liters per
minute to the right lung via the right lumen of the special tube. (anne)
Consider CPAP (5-10 cm H2O) to the collapsed, nondependent lung. This maintains patency of
the nondependent alveoli allowing gas exchange to occur and will divert blood away from the
collapsed lung.

•Continuous positive airway pressure (CPAP) 5 to 10 cmH2O to the nonventilated lung reduces
shunt fraction by providing oxygen to the circulation of the nonventilated lung [56]. This is used
only in response to hypoxemia, as any flow to the operative lung will cause partial inflation,
potentially worsening surgical exposure. High frequency jet ventilation to the nonventilated lung
has been used as an alternative to CPAP to improve oxygenation and decrease shunt [57]. A
bronchial blocker or FOB may be used to insufflate oxygen/CPAP into only the nonoperative
lobe(s) of the operative lung to treat hypoxemia

- simply: Provide oxygen to the collapsed lung (right lung) -> expansion - ventilation is
improved thus vq ratio improved
- increase ventilation of non-ventilated lung (right lung)

8. Medical student: Continue one lung ventilation but decrease the tidal volume from 600
ml to 300 ml. (Franco)
Low tidal volume — To minimize lung injury caused by high TVs, the standard of care at the
authors' institution is to use a TV of only 4 to 6 mL/kg predicted body weight during OLV
(adjusted from 6 to 8 mL/kg during two lung ventilation). This strategy is based on proven
benefits of low TV in critical care patients with previous lung injury, as well as some evidence of
benefit in those without lung injury. During low tidal volume ventilation, positive end-expiratory
pressure with or without recruitment maneuvers should be used to compensate for development
of atelectasis (loss of lung volume due to lung collapse). There is consensus that tidal volume
(VT) reduction to 6–8 mL per kg of predicted body weight improves the respiratory function and
reduces the incidence of Postoperative pulmonary complications.

600ml - high based on body weight - VQ relatively higher than normal

- super high tidal volume
- intralaveolar resistance went up due to the increase in tidal volume but the extraalveolar
resistance went down
- if maging 300ml - nearer to the functional residual capacity lowest point of PVR so there
will
- decrease this for a better vq ratio
- improved perfusion of left lung again
- high tidal volume of left lung -> diverted blood flow to the right lung